Background: CD8+ T‐cell activation, characterized by increased CD28 expression, reduces neointima formation after arterial injury in mice. The CD8+CD28hi phenotype is associated with increased effector function. In this study, we used a mouse model that has CD8+ but no CD4+ T cells (CD4−/−) to assess the role of CD8+ T cells and test the function of CD8+CD28hi T cells in modulating neointima formation after arterial injury. Methods and Results: Neointima formation after pericarotid arterial cuff injury was significantly less in CD4−/− mice compared with wild‐type (WT) mice. Negligible baseline lytic activity by splenic CD8+ T cells from uninjured WT mice against target syngeneic smooth muscle cells was significantly increased 7 days after injury. Interestingly, CD8+ T cells from uninjured CD4−/− mice had significant lytic activity at baseline that remained elevated 7 days after injury. CD8+ T‐cell lytic activity was significantly reduced by depletion of CD28hi cells. CD8+CD28hi T cells adoptively transferred into recipient Rag‐1−/− mice significantly reduced neointima formation compared with CD8+CD28+ T‐cell recipient mice. Conclusions: CD8+ T cells reduced neointima formation after arterial injury, attributed in part to increased function of the CD8+CD28hi phenotype.
JournaltitleJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease